Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 11, Pages 7102-7106Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.11.7102
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Funding
- NCRR NIH HHS [P20 RR021905] Funding Source: Medline
- NIAID NIH HHS [P01 AI045666, P01 AI045666-040003, P01 AI045666-030003, P01 AI045666-050001] Funding Source: Medline
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IL-6 trans-signaling via the soluble IL-6R (sIL-6R) plays an important role in the progression of several autoimmune diseases and cancer by providing IL-6-responsiveness to cells lacking IL-6R. However, the potential sources of sIL-6R are less understood. In this study we show that sIL-6R is produced by both naive and memory CD4 T cells upon TCR activation. The production of sIL-6R by activated CD4 T cells is mediated by shedding of the membrane-bound IL-6R, and this process correlates with the expression of the metalloproteinase ADAM17 in these cells. In contrast to CD4 T cells, CD8 T cells do not express ADAM17 and their production of sIL-6R is negligible. Thus, during an immune response CD4 T cells are an important source of sIL-6R. Production of sIL-6R by auto-reactive CD4 T cells may contribute to their role in the development of autoimmune disease by conferring IL-6-responsiveness to cells lacking IL-6R such as synoviocytes.
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